Severe esa resistance reversed by cinacalcet in a hemodialysis patient with sickle cell anemia

Introduction: Hematologic diseases such as sickle cell disease (SCD) complicate anemia of end-stage renal disease (ESRD). Hyperparathyroidism is another etiology of ESA resistance that can cause irreversible bone marrow fibrosis. We present a case of severe anema in a SCD patient on hemodialysis (HD) that dramatically improved with cinacalcet. Case Description: The patient is a 28 year old Black man with SCD and ESRD from FSGS on thrice weekly HD. His anemia had been treated with hydroxyurea and high dose subcutaneous Aranesp (400 μg every 2 weeks) with a mean hemoglobin (Hgb) of 6.4 (1.4) mg/dL over several years. He developed worsening hyperparathyroidism on phosphate binders and vitamin D. Despite stable Aranesp doses, Hgb decreased until a blood transfusion was needed. Aranesp was increased to 500 μg every 2 weeks with some increase in Hgb. After starting cinacalcet, parathyroid hormone (PTH) decreased (1390 to 593 pg/mL), and Hgb further increased (8.2 to 11.2 mg/dL). Intermittent nonadherence to cinacalcet led to PTH variability until hospital admissions for sickle cell crisis and then COVID-19. Afterwards, PTH was more consistently suppressed. Following day 500, supplemental Epogen was given in addition to Aranesp, but Hgb increased only when PTH was most suppressed. During the first year on cinacalcet, there was a strong inverse correlaton between Hgb and PTH (r=-0.6, p=.001). Figure 1 shows the Hgb, phosphorus, and PTH (divided by 150 to simplify y-axis) where Hgb peaks correspond to PTH nadirs. Discussion: We demonstrate a case of severe anemia from both ESRD and SCD where Hgb dramatically improved with cinacalcet. We acknowledge that Aranesp increases preceded the initial Hgb rise, but Hgb peaks following PTH suppression exceeded any prior levels. These Hgb peaks were reproducible and sustained whenever PTH suppression was achieved. This case demonstrates that some hyperparathyroidismrelated ESA resistance may be reversible and supports how important control of bone mineral disease is in specific populations of HD patients that are susceptible to severe anemia.